UK Biobank is a major prospective epidemiological study, including multimodal brain imaging, genetics and ongoing health outcomes. 1 key finding →
Participants: 8,428 Evidence: low
Full summary, score breakdown and related studies → Original source
27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
UK Biobank is a major prospective epidemiological study, including multimodal brain imaging, genetics and ongoing health outcomes. 1 key finding →
Participants: 8,428 Evidence: low
Full summary, score breakdown and related studies → Original source
Cerebrovascular dysregulation is a hallmark of Alzheimer's disease (AD), but the changes that occur in specific cell types have not been fully characterized. 1 key finding →
Participants: 220 Evidence: low
Full summary, score breakdown and related studies → Original source
There is currently little information available about how individual cell types contribute to Alzheimer's disease. 4 key findings →
Participants: 13,214 Evidence: low
Full summary, score breakdown and related studies → Original source
We used a collection of 708 prospectively collected autopsied brains to assess the methylation state of the brain's DNA in relation to Alzheimer's disease (AD). 2 key findings →
Participants: 117 Evidence: low
Full summary, score breakdown and related studies → Original source
Understanding the tissue-specific genetic controls of protein levels is essential to uncover mechanisms of post-transcriptional gene regulation. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The biological processes that are disrupted in the Alzheimer's disease (AD) brain remain incompletely understood. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by the selective vulnerability of specific neuronal populations, the molecular signatures of which are largely unknown. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by synaptic loss, which can result from dysfunctional microglial phagocytosis and complement activation. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Compared to individuals carrying two copies of the ε4 allele of apolipoprotein E (APOE), ε2 homozygotes have an approximate 99% reduction in late-onset Alzheimer's disease (AD) risk. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Exercise's protective effects in Alzheimer's disease (AD) are well recognized, but cell-specific contributions to this phenomenon remain unclear. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
The role of non-neuronal cells in Alzheimer's disease progression has not been fully elucidated. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Excitatory neurons are preferentially impaired in early Alzheimer's disease but the pathways contributing to their relative vulnerability remain largely unknown. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Complex diseases are characterized by spatiotemporal cellular and molecular changes that may be difficult to comprehensively capture. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is a complex neurodegenerative disease, perturbing neuronal and non-neuronal cell populations. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Genes play a strong role in Alzheimer's disease (AD), with late-onset AD showing heritability of 58-79% and early-onset AD showing over 90%. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Aging is the strongest risk factor for Alzheimer's disease (AD), although the underlying mechanisms remain unclear. 3 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterized by severe neuronal loss; however, the mechanisms by which neurons die remain elusive. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
To clarify the role of microglia in brain homeostasis and disease, an understanding of their maintenance, proliferation and turnover is essential. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Mitochondria vary in morphology and function in different tissues; however, little is known about their molecular diversity among cell types. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
A hallmark of all forms of Alzheimer's disease (AD) is an abnormal accumulation of the beta-amyloid protein (Abeta) in specific brain regions. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Amyotrophic lateral sclerosis (ALS) is a genetically heterogeneous neurodegenerative syndrome hallmarked by adult-onset loss of motor neurons. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →